Monday, April 18, 2016

VANCOUVER -- Guidelines for the use of botulinum toxin in various neurological disorders are getting an update, with the best evidence supporting the use of some formulations in spasticity and chronic migraine, researchers reported here.

All three botulinum toxin type A formulations are supported by level A evidence for use in upper limb spasticity, and onabotulinumtoxinA (Botox) received a level A recommendation in chronic migraine, although the magnitude of the benefit is small, according to David Simpson, MD, of Icahn School of Medicine at Mount Sinai in New York, and colleagues.

The new guidance, which is the first since 2008, was published online in Neurology and reported here at the American Academy of Neurology meeting.

There are four types of botulinum toxin available on the U.S. market: three type A and one type B. Type A botulinum toxins include abobotulinumtoxinA (Dysport), incobotulinumtoxinA (Xeomin), onabotulinumtoxinA (Botox), and the lone Type B product is rimabotulinumtoxinB (Myobloc).

Simpson and colleagues reviewed the evidence for botulinum toxin in four conditions: cervical dystonia, blephrospasm, limb spasticity, and headache.

"We chose these diseases because we had a sense that there were sufficient data to show they were going to change in particular ways," Mark Hallett, MD, of the National Insitute of Neurological Disorders and Stroke, a co-author of the guideline, said during a press briefing. "We already had a feeling for what we were going to find, but we had to prove it carefully."

All three botulinum toxin type A drugs had level-A evidence supporting their use in upper limb spasticity, and abobotulinumtoxinA and onabotulinumtoxinA had level A evidence behind their use in lower limb spasticity, the researchers reported.

There was also strong level-A evidence that onabotulinumtoxinA works in chronic migraine, since the drug had been approved by the FDA in 2010 for this condition -- although the magnitude of benefit was small, Simpson said, with a 15% reduction in headache days per month compared with placebo.

Monday, April 11, 2016

A new University of Virginia study suggests that many medical students and residents are racially biased in their pain assessment, and that their attitudes about race and pain correlate with falsely-held beliefs about supposed biological differences—like black people having thicker skin, or less sensitive nerve endings than white people—more generally.

The study highlights how a confluence of mistaken attitudes—about race, about biology, and about pain—can flourish in one of the worst possible places: medical schools where the future gatekeepers of relief are trained. And it illuminates what I've called the divided state of analgesia in America: overtreatment of millions of people that feeds painkiller abuse at the same time that, with far less public attention, millions of others are systematically undertreated. Think of it as a pain gap between the haves and the have-nots, along lines of class and race.

Unfortunately, the UVA findings are neither surprising nor fundamentally new. Back in the 1990s, two studies—one in an Atlanta emergency room, the other in Los Angeles—found that white patients being treated for long bone fractures were dosed more liberally than Latino patients in L.A., and more liberally than black ones in Atlanta. The authors put forward several possible explanations of the disparity: Perhaps patients in different groups expressed pain differently, or maybe caregivers interpreted pain differently in these groups, or perhaps nurses and doctors saw pain the same way across groups but just chose to remedy pain differently.

By the late 1990s, other studies found similar disparities in cancer care, where people receiving outpatient cancer care in places that mostly served minorities were three times more likely to be under-medicated with analgesics than patients in other settings. Speculation about the causes deepened: Perhaps inadequate prescribing for minority patients resulted from concerns about potential drug abuse, or maybe minority patients had more difficulty finding pharmacies that stocked opioid prescriptions, or again perhaps there was a cultural barrier in doctor-patient understanding and assessment. Into the 2000s, additional reports have confirmed the gap—again with no agreement about any single cause.